GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a transmembrane TNF receptor superfamily member that functions in immune regulation. GITR is expressed on CD4+CD25+ regulatory T cells (Treg) as well as on subsets of thymocytes, lymph node cells, and splenocytes, and it is upregulated on antigen-activated conventional CD4+ and CD8+ T cells. GITR binding by GITR Ligand/TNFSF18 costimulates the proliferation and activation of CD4+ or CD8+ conventional T cells. It also induces the proliferation of Treg but inhibits the ability of Treg to suppress immune responses. This can result in the development of autoimmunity, increased tumor cell killing by effector T cells, and increased inflammation in arthritis, allergic asthma, and inflammatory bowel disease. GITR is also expressed on sympathetic neurons where it enhances NGF-induced neurite outgrowth and branching.